Functional characterization of TRPM7 in nasopharyngeal carcinoma and its knockdown effects on tumorigenesis

Tumour Biol. 2016 Jul;37(7):9273-83. doi: 10.1007/s13277-015-4636-z. Epub 2016 Jan 15.

Abstract

The aim of this study was to evaluate the association of functional expression of TRPM7 with nasopharyngeal carcinoma (NPC) growth. We examined the correlation of TRPM7 expression with cell growth and proliferation, cell cycle, and apoptosis in vitro in NPC cell lines and NPC tumorigenesis in mice by conducting experiments in mice and by further analyzing the tumor volume and growth. We further explored to see whether there is any positive correlation with the TRPM7 knockdown in NPC cells with their sensitivity to radiation. We found that the functional expression of TRPM7 in nasopharyngeal carcinoma is a critical requirement for physiological processes such as cell cycle, resistance to apoptosis, and cell proliferation. TRPM7 knockdown also enhanced sensitivity to radiotherapy of nasopharyngeal carcinoma. Moreover, we identified TRPM7 as a novel potential regulator of cell proliferation in NPC, through signal transducer and activator of transcription 3 (STAT3)-mediated signaling pathway and other anti-apoptotic factors. TRPM7 and STAT3 activation might be critical for the growth of NPC cells and could be an effective target for treatment of nasopharyngeal carcinoma.

Keywords: Apoptosis; CNE-1 cells; Nasopharyngeal carcinoma; Prognosis; Radiotherapy; STAT3; TRPM7.

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Carcinogenesis / genetics*
  • Carcinogenesis / pathology
  • Carcinoma
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / genetics*
  • Nasopharyngeal Neoplasms / pathology
  • Protein Serine-Threonine Kinases / genetics*
  • STAT3 Transcription Factor / genetics
  • Signal Transduction / genetics
  • TRPM Cation Channels / genetics*
  • Tumor Burden / genetics

Substances

  • STAT3 Transcription Factor
  • TRPM Cation Channels
  • Protein Serine-Threonine Kinases
  • TRPM7 protein, human